C H R O N I C GASTRITIS-A
SIMPLE CLASSIFICATION
S. S. RAO,N. KRASNER AND T. J. THOMSON From the Departments of Pathology and Gastroenterology, Stobhill General Hospital, Glasgow Received 30 July 1974; Accepted 1 1 Oct. 1974
PLATES XLIV-XLIX A S IMPLE descriptive classification of chronic gastritis is recommended as follows : mild, moderately severe or severe chronic gastritis, with or without atrophy. To this basic classification may be added metaplasia if this is present. What is meant by the term " chronic gastritis "? In clinical concept it suggests chronic inflammatory change in the gastric mucosa, possibly caused by repeated irritation. To the pathologist, the term has carried different connotations and there is no general agreement on the histological classification of chronic gastritis. Magnus (1946) described chronic atrophic gastritis and diffuse atrophy of the gastric mucosa (non-inflammatory). Motteram (1951) subdivided chronic gastritis into (a) superficial gastritis with minimal gastric atrophy, (b) atrophic gastritis with moderate or severe atrophy and (c) gastric atrophy. Joske, Finkh and Wood (1955) classified chronic gastritis as slight, moderate or severe superficial gastritis, superficial gastritis with atrophy, atrophic gastritis, severe atrophic gastritis and gastric atrophy. In 1958 Wood and Taft used the terms superficial gastritis, atrophic gastritis and gastric a trophy. Of these authors, only Joske et al. referred to the degree of inflammatory cell infiltration and that was with reference to superficial gastritis. Recently Whitehead, Truelove and Gear (1972) based their classification on four features : (1) the mucosal type (body, pyloric, cardiac and transitional), (2) the grade of chronic gastritis, (3) the activity of gastritis and (4)the presence and type of metaplasia. The authors conceded that difficulties arise in recognising mucosal type when severe gastritis is associated with atrophy or metaplasia. The authors graded the degree of atrophy rather than the degree of chronic inflammatory cell infiltration. They reported the activity of the gastritis as positive or negative. Furthermore, they report that intestinal metaplasia nearly always occurs in a mucosa which is the site of atrophic gastritis. Based on these four criteria they recommended a somewhat complicated classification of chronic gastritis. The presence of auto-antibodies (gastric parietal cell and intrinsic factor) in association with chronic gastritis and Addisonian pernicious anaemia is well established (Wright et al., 1966). While little is known of the aetiology of chronic gastritis, various factors have been proposed by different authors Correspondence to: Dr S. S. Rao, Department of Pathology, Stobhill General Hospital, Glasgow, G21 3UW. J. PATH.-VOL.
117 (1975)
93
S. S. RAO, IV. KRASNER AND T. J . THOMSON
94
(Whitehead, 1973). A case can be made for making the term “ chronic gastritis ” a purely descriptive one unrelated to possible aetiological factors, especially when these are largely speculative. The “ chronic ” could reasonably be related to the histological finding of chronic inflammatory cell infiltration in the gastric mucosa. Siurala and Salim (1971) published evidence to support the view that gastric atrophy is a sequel to chronic gastritis. A statement regarding the presence or absence of atrophy would therefore also be meaningful. Using this simplified classification of gastritis, we examined gastric mucosal biopsies which had been taken from patients with a variety of upper gastrointestinal symptoms. MATERIALS AND METHODS Two hundred and forty-one patients were examined, their diagnoses including chronic peptic ulceration, gastric carcinoma and X-ray negative dyspepsia. Their ages ranged from 21 to 74 yr and there were 141 men and 100 women. Using the Olympus gastro-intestinal fiberscope Model GIF D, three to five gastric musocal biopsies were taken from each patient using Olympus forceps; the sites of the biopsies were in the pyloric antrum and at three levels-lower, middle and upper thirds of the body of the stomach. Each biopsy was laid on a piece of Whatman filter-paper, to assist orientation, and immediately fixed in 10 per cent. buffered formal saline and left overnight. Each was processed in a histokinetic tissue processor using the A16HR cycle and impregnated in paraplast. The tissue was carefully orientated before embedding it in fresh paraplast. Sections were made at three levels through the blocks and stained as follows : First level
(1) (2) Second level (3) (4) (5) Third level (6) (7) (8)
Haematoxylin and eosin Unstained Haematoxylin and eosin Unstained Haematoxylin and eosin Unstained Periodic acid Schiff (PAS) Gordon and Sweet’s silver impregnation of reticulin
The sections were examined by one of us (S. S. R.) without the knowledge of related clinical symptomatology.
RESULTS One hundred and eighty-four of the 241 patients had chronic gastritis. This diagnosis was made on finding chronic inflammatory cellular infiltration of the gastric mucosa, the infiltrate involving the full thickness of the mucosa in almost all instances. The inflammatory cell population consisted predominantly of lymphocytes and plasma cells, with a few eosinophils; in severe forms a few neutrophil polymorphs were also present. The chronic gastritis could be classified on two criteria, viz. (a) the degree of chronic inflammatory cell infiltration present, described as mild, moderately severe or severe and (b) the presence or absence of atrophy, referring to either the glands or to the mucosa as a whole. The gastric biopsies in 28 patients showed a mild degree of chronic inflammatory cell infiltration, mainly of plasma cells and lymphocytes, involving the full thickness of gastric mucosa, the superficial part of which contained a higher proportion of plasma cells. Five of them showed atrophy (figs. 1 and 2), while
CHRONIC GASTRITIS
95
23 did not (figs. 3 and 4). In 88 patients the biopsies showed moderately severe chronic inflammatory cell infiltration of the full thickness of gastric mucosa, the infiltration consisting of lymphocytes, plasma cells and a few eosinophils. Atrophy was present in 23 of these (figs. 5 and 6) and absent in 65 (figs. 7 and S). Sixty-eight patients had severe chronic inflammatory cell infiltration of the full thickness of gastric mucosa. In addition to lymphocytes, plasma cells and eosinophils, there were also a few neutrophil polymorphs in the inflammatory cell infiltration. Thirty-nine demonstrated loss of glands and atrophy of the gastric mucosa (figs. 9 and lo), while 29 showed no atrophy (figs.11 and 12). Intestinal metaplasia and/or pseudopyloric metaplasia of gastric mucosa was seen in several biopsies showing chronic gastritis with atrophy. In only three patients was true superficial gastritis seen, where the chronic inflammatory cell infiltration was limited to the lamina propria between gastric pits. The connective tissue in between the deep glands was free of inflammatory cells.
DISCUSSION The term chronic gastritis carries different connotations for the clinician, pathologist and radiologist. There have been many published classifications of chronic gastritis which have been based on the degree of atrophy of the mucosa and the severity of the inflammatory cell infiltration in the lamina propria between the gastric pits. Little attention has been given to the degree of chronic inflammatory cell infiltration involving the full thickness of the gastric mucosa. In this communication we support the use of terms which are descriptive of the morphological abnormalities found in mucosal biopsies, namely the degree of infiltration of the whole gastric mucosa by chronic inflammatory cells and the presence or absence of atrophy. Being purely descriptive, such terminology simplifies the classification, and minimises observer error. The presence or absence of metaplasia can be added to the basic classification. Morson (1955) investigated intestinal metaplasia in gastric mucosa of patients with duodenal ulcers, gastric ulcers and gastric carcinomas. He found that intestinal metaplasia was present in all three groups, and it occurred most frequently and extensively in the pyloric antrum and the lesser curve of the stomach. Magnus (1937) and Schindler (1947) believed that intestinal metaplasia was due to repeated damage of mucosa by gastritis. Warren and Meissner (1944) regard it as the chief epithelial feature of chronic gastritis. It is recognised that other uncommon forms of chronic gastritis are seen from time to time but these carry descriptive adjectives such as follicular, chronic cystic, eosinophilic or hypertrophic gastritis. Superficial gastritis is not as common as has been previously reported. Ylvisker et al. (1955) found a comparatively low incidence of superficial gastritis in their series. Many of the photomicrographs which appear in the medical literature labelled as “ superficial gastritis” show inflammatory cell infiltration involving the full thickness of the gastric mucosa, and in some cases even extending beyond the muscularis mucosa. Many of the so-called cases of “ superficial gastritis ” are examples of mild, moderately severe or severe chronic gastritis without atrophy.
96
S. S. RAO, N. KRASNER AND T. J. THOMSON
Gastric atrophy is said to be the end stage of atrophic gastritis (Whitehead, 1973) or associated with Addisonian pernicious anaemia. As there is virtually no inflammatory cell infiltration but only atrophy, we do not consider it justifiable to include gastric atrophy in the classification of chronic gastritis. This is a very simple classification of chronic gastritis based on subjective assessment of the degree of chronic inflammatory infiltration and atrophy of mucosal glands. No attempt is made to relate the different types to each other as possible stages in the same process. This classification can be applied to gastric mucosa irrespective of the site from which it has been taken. From a purely descriptive point of view it might be of some value, if only to resolve some of the confusion in terminology in this field. SUMMARY Gastric mucosal biopsy specimens from 241 patients were examined. Chronic inflammatory cellular infiltration of the gastric mucosa was found in 181 patients and this graded as mild, moderate or severe. The presence or absence of atrophy or intestinal metaplasia was noted. True superficial gastritis was observed in only three cases. We would like to thank Mr P. S. Waldie and the staff of the Audio Visual Services Department for the preparation of the photomicrographs. REFERENCES JOSKE,R. A., FINKH, E. S., AND WOOD,I. J. 1955. Gastric biopsy : A study of 1000 consecutive successful gastric biopsies. Quart. J. Med., 24, 269. MAGNUS, H. A. 1937. Observations on the presence of intestinal epithelium in the gastric mucosa. J. Path. Bact., 44, 389. MAGNUS, H. A. 1946. The pathology of simple gastritis. J. Path. Bact., 58, 431. MORSON,B. C. 1955. Intestinal metaplasia of the gastric mucosa. Brit. J. Cancer, 9, 365. R. 1951. Biopsy study of chronic gastritis and gastric atrophy. J . Path. Bact., MOTTERAM, 63,389. SCHINDLER, R. 1947. Gastritis. London, Heinemann. SIURALA,M., AND SALIM,H. J. 1971. Long term follow-up of subjects with superficial gastritis or a normal gastric mucosa. Scand. J. Gastroent., 6,459. WARREN, S.,AND MEISSNER, W. A. 1944. Chronic gastritis and carcinoma of the stomach. Gastroenterology, 3,25 1. R., TRUELOVE, S. C., AND GEAR,M. W. 1972. The histological diagnosis of WHITEHEAD, chronic gastritis in fibreotic gastroscope biopsy specimens. J. Clin. Path., 25, 1. WHITEHEAD, R. 1973. Mucosal biopsy of the gastrointestinal tract. W. B. Saunders Co. Ltd., Philadelphia p. 33. R., WANGEL, A. G., SALEM, S. M., AND SCHILLER, K. F. N. 1966. WRIGHT,R., WHITEHEAD, Autoantibodies and microscopic appearances of gastric mucosa. Lancet, 1, 618 YLVISKER,R. S., CAREY,J. B. SR., MYHNE,J., AND CAREY,J. B. JR. 1955. Biopsy studies of gastric mucosa. Gastroenterology, 28, 88.
PLATEXLlV
RAO, KKASNER AND THOMSON
CHRONIC GASTRITIS
FIG. 1 .-Mild chronic gastritis with atrophy. In addition to mild chronic inflammatory cell infiltration involving the full thickness of gastric mucosa there is atrophy and loss of glands as well as intestinal metaplasia. Haematoxylin and eosin (HE). x 430.
FIG.2.-Mild
chronic gastritis with atrophy. Reticulin stain of fig. 2 confirming loss of glands and atrophy of mucosa. x 430.
PLATEXLV
RAO, KRASNERAND THOMSON CHRONIC GASTRITIS
FIG.3.-Mild chronic gastritis with no atrophy. Mild chronic inflammatory cell infiltration of pyloric-type of gastric mucosa involving the full thickness, but no loss of glands or atrophy. HE. x430.
FIG.4.-Mild chronic gastritis with no atrophy. Reticulin stains of fig. 4 confirming no loss of the glands or atrophy of gastric mucosa. x 430.
PLATEXLVI
RAO, KRASNER AND THOMSON CHRONIC GASTRITIS
FIG.5.-Moderately severe chronic gastritis with atrophy. In addition to moderately severe chronic inflammatory cell infiltration involving the full thickness of gastric mucosa, there is loss of glands and atrophy, as well as intestinal metaplasia. HE. x 430.
FIG. 6.-Moderately
severe chronic gastritis with atrophy. Reticulin stain of fig. 6 confirming atrophy of the gastric mucosa with loss of glands. x 430.
PLATEXLVII
RAO, KRASNER AND THOMSON CHRONIC GASTRITIS
FIG.7.-Moderately severe chronic gastritis with no atrophy. There is moderately severe chronic inflammatory cell infiltration involving the full thickness of the mucosa; but no atrophy or loss of glands. HE. x430.
FIG.8.-Moderately severe chronic gastritis with no atrophy. Reticulin stain of fig. 8 confirming that-there is no loss of glands or atrophy of gastric mucosa. x 430.
PLATEXLVlII
RAO, KKASNER AND THOMSON CHRONIC GASTRlTlS
FIG. 9.-Severe chronic gastritis with atrophy. Severe chronic inflammatory cell infiltration together with a few neutrophilic polymorphs involving the full thickness of the gastric mucosa. There is loss of glands and atrophy of the mucosa. HE. x 430.
FIG. lO.--Severe chronic gastritis with atrophy. Reticulin stain of fig. 10 confirming atrophy of gastric mucosa with loss of glands. x 430.
RAO, KRASNER
AND
PLATEXLTX
THOMSON CHRONIC GASTRITIS
FIG. 1 1 .-Severe chronic gastritis with no atrophy. Severe chronic inflammatory cell infiltration involving full thickness of the gastric mucosa. Also a few small foci of neutrophilic polymorph infiltration are present. There is no loss of glands or atrophy of the mucosa. HE. x 430.
FIG.12.-Severe
chronic gastritis with no atrophy. Reticulin stain of fig. 12 confirming no atrophy or loss of glands. x 430.
SIMPLE CLASSIFICATION
S. S. RAO,N. KRASNER AND T. J. THOMSON From the Departments of Pathology and Gastroenterology, Stobhill General Hospital, Glasgow Received 30 July 1974; Accepted 1 1 Oct. 1974
PLATES XLIV-XLIX A S IMPLE descriptive classification of chronic gastritis is recommended as follows : mild, moderately severe or severe chronic gastritis, with or without atrophy. To this basic classification may be added metaplasia if this is present. What is meant by the term " chronic gastritis "? In clinical concept it suggests chronic inflammatory change in the gastric mucosa, possibly caused by repeated irritation. To the pathologist, the term has carried different connotations and there is no general agreement on the histological classification of chronic gastritis. Magnus (1946) described chronic atrophic gastritis and diffuse atrophy of the gastric mucosa (non-inflammatory). Motteram (1951) subdivided chronic gastritis into (a) superficial gastritis with minimal gastric atrophy, (b) atrophic gastritis with moderate or severe atrophy and (c) gastric atrophy. Joske, Finkh and Wood (1955) classified chronic gastritis as slight, moderate or severe superficial gastritis, superficial gastritis with atrophy, atrophic gastritis, severe atrophic gastritis and gastric atrophy. In 1958 Wood and Taft used the terms superficial gastritis, atrophic gastritis and gastric a trophy. Of these authors, only Joske et al. referred to the degree of inflammatory cell infiltration and that was with reference to superficial gastritis. Recently Whitehead, Truelove and Gear (1972) based their classification on four features : (1) the mucosal type (body, pyloric, cardiac and transitional), (2) the grade of chronic gastritis, (3) the activity of gastritis and (4)the presence and type of metaplasia. The authors conceded that difficulties arise in recognising mucosal type when severe gastritis is associated with atrophy or metaplasia. The authors graded the degree of atrophy rather than the degree of chronic inflammatory cell infiltration. They reported the activity of the gastritis as positive or negative. Furthermore, they report that intestinal metaplasia nearly always occurs in a mucosa which is the site of atrophic gastritis. Based on these four criteria they recommended a somewhat complicated classification of chronic gastritis. The presence of auto-antibodies (gastric parietal cell and intrinsic factor) in association with chronic gastritis and Addisonian pernicious anaemia is well established (Wright et al., 1966). While little is known of the aetiology of chronic gastritis, various factors have been proposed by different authors Correspondence to: Dr S. S. Rao, Department of Pathology, Stobhill General Hospital, Glasgow, G21 3UW. J. PATH.-VOL.
117 (1975)
93
S. S. RAO, IV. KRASNER AND T. J . THOMSON
94
(Whitehead, 1973). A case can be made for making the term “ chronic gastritis ” a purely descriptive one unrelated to possible aetiological factors, especially when these are largely speculative. The “ chronic ” could reasonably be related to the histological finding of chronic inflammatory cell infiltration in the gastric mucosa. Siurala and Salim (1971) published evidence to support the view that gastric atrophy is a sequel to chronic gastritis. A statement regarding the presence or absence of atrophy would therefore also be meaningful. Using this simplified classification of gastritis, we examined gastric mucosal biopsies which had been taken from patients with a variety of upper gastrointestinal symptoms. MATERIALS AND METHODS Two hundred and forty-one patients were examined, their diagnoses including chronic peptic ulceration, gastric carcinoma and X-ray negative dyspepsia. Their ages ranged from 21 to 74 yr and there were 141 men and 100 women. Using the Olympus gastro-intestinal fiberscope Model GIF D, three to five gastric musocal biopsies were taken from each patient using Olympus forceps; the sites of the biopsies were in the pyloric antrum and at three levels-lower, middle and upper thirds of the body of the stomach. Each biopsy was laid on a piece of Whatman filter-paper, to assist orientation, and immediately fixed in 10 per cent. buffered formal saline and left overnight. Each was processed in a histokinetic tissue processor using the A16HR cycle and impregnated in paraplast. The tissue was carefully orientated before embedding it in fresh paraplast. Sections were made at three levels through the blocks and stained as follows : First level
(1) (2) Second level (3) (4) (5) Third level (6) (7) (8)
Haematoxylin and eosin Unstained Haematoxylin and eosin Unstained Haematoxylin and eosin Unstained Periodic acid Schiff (PAS) Gordon and Sweet’s silver impregnation of reticulin
The sections were examined by one of us (S. S. R.) without the knowledge of related clinical symptomatology.
RESULTS One hundred and eighty-four of the 241 patients had chronic gastritis. This diagnosis was made on finding chronic inflammatory cellular infiltration of the gastric mucosa, the infiltrate involving the full thickness of the mucosa in almost all instances. The inflammatory cell population consisted predominantly of lymphocytes and plasma cells, with a few eosinophils; in severe forms a few neutrophil polymorphs were also present. The chronic gastritis could be classified on two criteria, viz. (a) the degree of chronic inflammatory cell infiltration present, described as mild, moderately severe or severe and (b) the presence or absence of atrophy, referring to either the glands or to the mucosa as a whole. The gastric biopsies in 28 patients showed a mild degree of chronic inflammatory cell infiltration, mainly of plasma cells and lymphocytes, involving the full thickness of gastric mucosa, the superficial part of which contained a higher proportion of plasma cells. Five of them showed atrophy (figs. 1 and 2), while
CHRONIC GASTRITIS
95
23 did not (figs. 3 and 4). In 88 patients the biopsies showed moderately severe chronic inflammatory cell infiltration of the full thickness of gastric mucosa, the infiltration consisting of lymphocytes, plasma cells and a few eosinophils. Atrophy was present in 23 of these (figs. 5 and 6) and absent in 65 (figs. 7 and S). Sixty-eight patients had severe chronic inflammatory cell infiltration of the full thickness of gastric mucosa. In addition to lymphocytes, plasma cells and eosinophils, there were also a few neutrophil polymorphs in the inflammatory cell infiltration. Thirty-nine demonstrated loss of glands and atrophy of the gastric mucosa (figs. 9 and lo), while 29 showed no atrophy (figs.11 and 12). Intestinal metaplasia and/or pseudopyloric metaplasia of gastric mucosa was seen in several biopsies showing chronic gastritis with atrophy. In only three patients was true superficial gastritis seen, where the chronic inflammatory cell infiltration was limited to the lamina propria between gastric pits. The connective tissue in between the deep glands was free of inflammatory cells.
DISCUSSION The term chronic gastritis carries different connotations for the clinician, pathologist and radiologist. There have been many published classifications of chronic gastritis which have been based on the degree of atrophy of the mucosa and the severity of the inflammatory cell infiltration in the lamina propria between the gastric pits. Little attention has been given to the degree of chronic inflammatory cell infiltration involving the full thickness of the gastric mucosa. In this communication we support the use of terms which are descriptive of the morphological abnormalities found in mucosal biopsies, namely the degree of infiltration of the whole gastric mucosa by chronic inflammatory cells and the presence or absence of atrophy. Being purely descriptive, such terminology simplifies the classification, and minimises observer error. The presence or absence of metaplasia can be added to the basic classification. Morson (1955) investigated intestinal metaplasia in gastric mucosa of patients with duodenal ulcers, gastric ulcers and gastric carcinomas. He found that intestinal metaplasia was present in all three groups, and it occurred most frequently and extensively in the pyloric antrum and the lesser curve of the stomach. Magnus (1937) and Schindler (1947) believed that intestinal metaplasia was due to repeated damage of mucosa by gastritis. Warren and Meissner (1944) regard it as the chief epithelial feature of chronic gastritis. It is recognised that other uncommon forms of chronic gastritis are seen from time to time but these carry descriptive adjectives such as follicular, chronic cystic, eosinophilic or hypertrophic gastritis. Superficial gastritis is not as common as has been previously reported. Ylvisker et al. (1955) found a comparatively low incidence of superficial gastritis in their series. Many of the photomicrographs which appear in the medical literature labelled as “ superficial gastritis” show inflammatory cell infiltration involving the full thickness of the gastric mucosa, and in some cases even extending beyond the muscularis mucosa. Many of the so-called cases of “ superficial gastritis ” are examples of mild, moderately severe or severe chronic gastritis without atrophy.
96
S. S. RAO, N. KRASNER AND T. J. THOMSON
Gastric atrophy is said to be the end stage of atrophic gastritis (Whitehead, 1973) or associated with Addisonian pernicious anaemia. As there is virtually no inflammatory cell infiltration but only atrophy, we do not consider it justifiable to include gastric atrophy in the classification of chronic gastritis. This is a very simple classification of chronic gastritis based on subjective assessment of the degree of chronic inflammatory infiltration and atrophy of mucosal glands. No attempt is made to relate the different types to each other as possible stages in the same process. This classification can be applied to gastric mucosa irrespective of the site from which it has been taken. From a purely descriptive point of view it might be of some value, if only to resolve some of the confusion in terminology in this field. SUMMARY Gastric mucosal biopsy specimens from 241 patients were examined. Chronic inflammatory cellular infiltration of the gastric mucosa was found in 181 patients and this graded as mild, moderate or severe. The presence or absence of atrophy or intestinal metaplasia was noted. True superficial gastritis was observed in only three cases. We would like to thank Mr P. S. Waldie and the staff of the Audio Visual Services Department for the preparation of the photomicrographs. REFERENCES JOSKE,R. A., FINKH, E. S., AND WOOD,I. J. 1955. Gastric biopsy : A study of 1000 consecutive successful gastric biopsies. Quart. J. Med., 24, 269. MAGNUS, H. A. 1937. Observations on the presence of intestinal epithelium in the gastric mucosa. J. Path. Bact., 44, 389. MAGNUS, H. A. 1946. The pathology of simple gastritis. J. Path. Bact., 58, 431. MORSON,B. C. 1955. Intestinal metaplasia of the gastric mucosa. Brit. J. Cancer, 9, 365. R. 1951. Biopsy study of chronic gastritis and gastric atrophy. J . Path. Bact., MOTTERAM, 63,389. SCHINDLER, R. 1947. Gastritis. London, Heinemann. SIURALA,M., AND SALIM,H. J. 1971. Long term follow-up of subjects with superficial gastritis or a normal gastric mucosa. Scand. J. Gastroent., 6,459. WARREN, S.,AND MEISSNER, W. A. 1944. Chronic gastritis and carcinoma of the stomach. Gastroenterology, 3,25 1. R., TRUELOVE, S. C., AND GEAR,M. W. 1972. The histological diagnosis of WHITEHEAD, chronic gastritis in fibreotic gastroscope biopsy specimens. J. Clin. Path., 25, 1. WHITEHEAD, R. 1973. Mucosal biopsy of the gastrointestinal tract. W. B. Saunders Co. Ltd., Philadelphia p. 33. R., WANGEL, A. G., SALEM, S. M., AND SCHILLER, K. F. N. 1966. WRIGHT,R., WHITEHEAD, Autoantibodies and microscopic appearances of gastric mucosa. Lancet, 1, 618 YLVISKER,R. S., CAREY,J. B. SR., MYHNE,J., AND CAREY,J. B. JR. 1955. Biopsy studies of gastric mucosa. Gastroenterology, 28, 88.
PLATEXLlV
RAO, KKASNER AND THOMSON
CHRONIC GASTRITIS
FIG. 1 .-Mild chronic gastritis with atrophy. In addition to mild chronic inflammatory cell infiltration involving the full thickness of gastric mucosa there is atrophy and loss of glands as well as intestinal metaplasia. Haematoxylin and eosin (HE). x 430.
FIG.2.-Mild
chronic gastritis with atrophy. Reticulin stain of fig. 2 confirming loss of glands and atrophy of mucosa. x 430.
PLATEXLV
RAO, KRASNERAND THOMSON CHRONIC GASTRITIS
FIG.3.-Mild chronic gastritis with no atrophy. Mild chronic inflammatory cell infiltration of pyloric-type of gastric mucosa involving the full thickness, but no loss of glands or atrophy. HE. x430.
FIG.4.-Mild chronic gastritis with no atrophy. Reticulin stains of fig. 4 confirming no loss of the glands or atrophy of gastric mucosa. x 430.
PLATEXLVI
RAO, KRASNER AND THOMSON CHRONIC GASTRITIS
FIG.5.-Moderately severe chronic gastritis with atrophy. In addition to moderately severe chronic inflammatory cell infiltration involving the full thickness of gastric mucosa, there is loss of glands and atrophy, as well as intestinal metaplasia. HE. x 430.
FIG. 6.-Moderately
severe chronic gastritis with atrophy. Reticulin stain of fig. 6 confirming atrophy of the gastric mucosa with loss of glands. x 430.
PLATEXLVII
RAO, KRASNER AND THOMSON CHRONIC GASTRITIS
FIG.7.-Moderately severe chronic gastritis with no atrophy. There is moderately severe chronic inflammatory cell infiltration involving the full thickness of the mucosa; but no atrophy or loss of glands. HE. x430.
FIG.8.-Moderately severe chronic gastritis with no atrophy. Reticulin stain of fig. 8 confirming that-there is no loss of glands or atrophy of gastric mucosa. x 430.
PLATEXLVlII
RAO, KKASNER AND THOMSON CHRONIC GASTRlTlS
FIG. 9.-Severe chronic gastritis with atrophy. Severe chronic inflammatory cell infiltration together with a few neutrophilic polymorphs involving the full thickness of the gastric mucosa. There is loss of glands and atrophy of the mucosa. HE. x 430.
FIG. lO.--Severe chronic gastritis with atrophy. Reticulin stain of fig. 10 confirming atrophy of gastric mucosa with loss of glands. x 430.
RAO, KRASNER
AND
PLATEXLTX
THOMSON CHRONIC GASTRITIS
FIG. 1 1 .-Severe chronic gastritis with no atrophy. Severe chronic inflammatory cell infiltration involving full thickness of the gastric mucosa. Also a few small foci of neutrophilic polymorph infiltration are present. There is no loss of glands or atrophy of the mucosa. HE. x 430.
FIG.12.-Severe
chronic gastritis with no atrophy. Reticulin stain of fig. 12 confirming no atrophy or loss of glands. x 430.
